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Objective: To assess the practicability and monitor the results of an active carrier testing program among relatives of cystic fibrosis (CF) patients., Methods: Parents of CF patients in the Veneto and Trentino regions of northeastern Italy were asked to help recruit relatives aged between 18 and 45 years for CF mutation testing., Results: Of 409 enrolled CF parents, 59.6% agreed to send to the CF Center family composition data of relatives up to the third degree, and 28.8% recruited relatives to carrier testing, providing names and addresses of those who, being contacted, expressed a willingness to be tested. The participation of parents was higher if they were young and had a child recently diagnosed with CF. Recruiting parents indicated 333 close relatives (59%) for testing. When contacted by the CF Center, 170 of these 333 (51%) attended for testing. The percentage of close relatives who spontaneously asked for the test was 5.4% before the carrier testing program started; it rose to 25.3% following the introduction of the active strategy., Conclusions: The participation of the parents of CF patients is an important factor affecting the utilization of testing by relatives. Besides this, the influence of a favorable medical and cultural context (participation of gynecologists and family doctors in testing programs, genetic education of the general population) has to be considered., (Copyright 2000 S. Karger AG, Basel)

Background: The FAMIS (Fosinopril in Acute Myocardial Infarction Study) was a multicenter, placebo-controlled, double-blind trial designed to evaluate the safety and the efficacy of fosinopril in reducing left ventricular enlargement after acute anterior myocardial infarction. We evaluated the echocardiographic examinations performed during the trial in order to assess the trend of the remodeling process over time and to evaluate the role of infarct size in identifying patients at risk of progressive left ventricular dilation., Methods: A complete echocardiographic examination was performed on admission, before discharge and three months later. Patients undergoing coronary bypass surgery or PTCA had a further examination prior to the procedure. The echocardiograms were analyzed at a central laboratory, and the end-diastolic and end-systolic left ventricular volumes were computed by using a modified Simpson's rule technique. Regional wall motion was evaluated using the centerline method, analyzing the left ventricular boundary along 100 chords perpendicular to the centerline constructed midway between the end-diastolic and the end-systolic contours. A quantitative infarct-size index was then computed according to the number of chords with a fractional shortening equal to or less than 5%., Results: Left ventricular end-diastolic and end-systolic volume index significantly increased over time (p < 0.0001); as a result, the stroke volume increased (p < 0.0001) but the ejection fraction did not change. Patients were then divided according to the three-month infarct-size index. For both end-diastolic and end-systolic volume, not only did larger infarcts had higher volumes, but there was also a greater increase from baseline to 3 months. Moreover, larger infarcts had a lower ejection fraction, with a further reduction over the three months, while smaller infarcts had higher values and an increase over time. An infarct-size index of 25 or larger allowed prospective identification at the baseline examination of patients at risk of subsequent left ventricular dilation., Conclusions: In conclusion, patients at greatest risk of left ventricular dilation, namely those with larger infarct size, constitute a group that is worth considering for any therapeutic effort for reducing the remodeling process. These patients could in fact benefit from therapeutic strategies aimed at the reduction of left ventricular remodeling and should be studied in clinical trials.

Measurement of levels of exhaled nitric oxide (NO) has been proposed as a noninvasive method for evaluating the degree of airway inflammation in asthmatic patients. Some concern in the interpretation of results of such measurement may arise from possible interference by high environmental concentrations of NO inhaled by these patients. The aim of this study was to verify whether environmental concentrations of NO in the range from 0 to 150 ppb can influence levels of exhaled NO. We tested two groups of subjects. The first group, consisting of 16 subjects, was tested when environmental levels of NO were from 0 to 3 ppb and from 20 to 60 ppb, and exhaled NO mean ppb (+/- SEM) levels were 9.81 +/- 1.43 and 9.78 +/- 1.47 (p = ns) (mean +/- SEM), respectively. The second group, consisting of 30 subjects, was tested at ambient NO concentrations of 0 to 3 ppm, 80 to 100 ppm, and 120 to 150 ppb, and for 18 of these subjects who underwent testing under all three conditions investigated, the mean levels of exhaled NO were 9.23 +/- 1.51, 7.78 +/- 1.19, and 9.33 +/- 1.55 ppb (p = ns), respectively. The results of this study suggest that significantly different ambient levels of NO have no effect on levels of exhaled NO.

Revascularization can improve ventricular function in patients with viable myocardium, but whether and how the presence of viable myocardium affects prognosis of infarcted patients is still far from clear. Thus, 202 patients (173 men, 59 +/- 9 years old) with a previous or recent myocardial infarction (MI) and regional asynergies underwent low-dose dobutamine echocardiography (5-15 microg/kg per min) to assess myocardial viability and were followed for a period of 16 +/- 11 months after revascularization (89 patients) or medical therapy (113 patients). Four groups of patients were defined: (1) patients with viability, revascularized (n = 64); (2) patients with viability, treated medically (n = 52); (3) patients without viability, revascularized (n = 25); and (4) patients without viability, treated medically (n = 61). Of these patients, 45 (23%) patients suffered 57 cardiac events: 18 cardiac deaths (9%), 7 MIs, 12 unstable angina, 9 heart failures, and 11 new revascularization procedures. Patients with viability, revascularized, experienced a slightly lower event rate (22%) compared with patients with viability, treated medically, patients without viability, treated medically and patients without viability, revascularized (29%, 31%, and 36%, respectively; p = not significant [NS]). The frequency of events was then evaluated in those 108 patients with an ejection fraction < or =33%, in whom 14 cardiac deaths occurred: the incidence of cardiac death was slightly lower in patients with viability, revascularized (3/37, 8%) than in the patients with viability, treated medically (4/26, 15%), patients without viability, revascularized (2/11, 18%), or patients without viability, treated medically (5/34, 15%) (p = NS). Nonfatal cardiac events were significantly fewer (p <0.05) in patients with viability, revascularized (8%) and in patients without viability, treated medically (6%) than in patients with viability, treated medically and patients without viability, revascularized (27%). In infarcted patients with severe left ventricular dysfunction, the presence of viable myocardium, if left unrevascularized, leads to further events. On the contrary, in the absence of myocardial viability, revascularization could lead to a worse prognosis than medical therapy.

The values of apolipoproteins (apo) A-I and B were determined in a population sample of hospital outpatients with a standardized method to verify if the cutpoints calculated in a cross-sectional study in the US are usable with other populations. We also tested the apolipoproteins' ability to discriminate between healthy people and survivors of myocardial infarction. In the studied population the apo A-I value corresponding to the HDL-cholesterol decisional centile is 1.12 g/L for males and 1.17 g/L for females; the apo B value corresponding to the LDL-cholesterol decisional centile is 1.23 g/L for males and 1.14 g/L for females. These values are quite close to the cutpoints proposed for the American population (1.20 g/L for both apolipoproteins). In comparison with the LDL- and HDL-cholesterol decisional concentrations, the cutpoints for apolipoproteins allow a correct classification of a greater percentage of postmyocardial infarction patients (16% higher for apo B and 5% for apo A-I). Standardized assays coupled with a reference database allow a better clinical use of apolipoprotein measurements.

In order to compare the efficacy of nifedipine gastrointestinal therapeutic system (GITS) with diltiazem, 99 patients with chronic stable angina were studied in a parallel-group randomised trial. According to the results of the two exercise tolerance tests (ETTs) performed during the placebo run-in, patients were divided into a fixed threshold group if the variability in time to 1 mm ST-segment depression was 20%, or a variable threshold group if it was higher. Efficacy was assessed by comparing the time to 1 mm ST-depression on a bicycle ETT after 4 weeks of treatment, adjusting for the baseline value. The adjusted means were 7.44 min for nifedipine GITS and 7.68 min for diltiazem; the difference was -0.24 min, with a lower 90% confidence limit of -0.90, which is within the stated interval for equivalence. The same result was confirmed by the 'intention-to-treat' analysis, and comparable results were obtained both in fixed and in variable threshold groups. The incidence of side effects was 12% with nifedipine GITS and 8.2% with diltiazem. Nifedipine GITS and diltiazem were found to be equally effective in increasing exercise tolerance in chronic stable angina patients.

In the assessment of the acute results of percutaneous transluminal coronary angioplasty (PTCA), myocardial perfusion at maximal vasodilatation theoretically has fewer limitations than the coronary flow reserve measurements and quantitative coronary angiography. The purpose of this study was to compare the myocardial perfusion to the measurements of the severity of the lesion (minimal luminal diameter and percent area stenosis) and to relate it to the changes of left ventricular function after PTCA. Regional myocardial perfusion was assessed during intracoronary papaverine, using the inverse mean transit time of contrast medium (1/Tmn), before, 15 min after, 18-24 hr after, and 6 months after successful single-vessel PTCA in 14 patients with stable angina. Left ventricular angiography (before angioplasty, 18-24 hr after, and 6 months later) was analysed by area-length and centerline methods. Immediately after PTCA, 1/Tmn increased from 0.14 +/- 0.07 sec-1 to 0.21 +/- 0.09 sec-1 (P = .001). Maximal myocardial perfusion remained higher than the pre-PTCA value the day after angioplasty (1/Tmn of 0.23 +/- 0.09 sec-1), while it reduced to near pre-PTCA values at follow-up (1/Tmn of 0.16 +/- 0.05 sec-1). Before PTCA, three out of ten patients had ejection fraction of < 65%, and seven had mild-to-moderate hypokinesis. The day after PTCA the ejection fraction and the regional dysfunction improved significantly. The change in ejection fraction 18-24 hr after PTCA did not correlate with minimal luminal diameter and percent area stenosis and correlated slightly with the improvement of perfusion (r = 0.54, P = .10). At follow-up left ventricular function deteriorated in the whole group, despite the persistence of angiographic success of PTCA, possibly because of changes in the loading condition. Coronary artery stenosis measurements and 1/Tmn failed to correlate with the left ventricular function. Given the difficulties in routine application of the analysis of time-density curves, the measurement of minimal luminal diameter remains a more practical assessment of the results of the intervention. However, the improvement of myocardial perfusion may give more information than coronary artery dimensions of the early recovery of left ventricular function.

Background: Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction)., Methods: Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment., Results: In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not., Conclusions: Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.

Since late eighties, large clinical trials on thrombolytic therapy have introduced in cardiology literature the use of survival measures in order to assess the consequences of treatment. In this article a systematic review of the more frequently adopted measures is presented, together with the proposal of other measures, more useful for the clinician.

Variations of serum and nasal specific IgE to Dermatophagoides pteronyssinus (Der p) during alternate periods of antigen avoidance-exposure have been evaluated with an open design in a group of allergic children with asthma and rhinitis at the residential house Istituto Pio XII (Misurina, BL, Italy), at 1756 m, in the Italian Dolomites. A method based on direct incubation of allergen coupled substrate on the nasal mucosa has been employed to evaluate the levels of nasal IgE. Serum specific IgE decreased respectively from (median) 117-89.3 kU/l (P < 0.001) during an initial period of 3 months of allergen avoidance and from 88.2 to 78.4 kU/l (P < 0.0002) during a subsequent period of allergen avoidance. No significant increase in serum specific IgE was, in contrast, observed during two periods, 22 and 9 days, of antigen exposure, changing respectively from 89.3 to 88.2 and from 78.4 to 89.1 kU/l. In contrast, nasal IgE has been significantly influenced by the alternate periods of antigen exposure-avoidance, showing a decrease from 19.75 to 4.01 kU/l (P < 0.0001) after the initial period of avoidance, followed by an increase to 9.95 kU/l (P < 0.0001) after 22 days of exposure. A significant decrease to a value of 2.37 kU/l (P < 0.0001) was also observed during the subsequent period of avoidance, followed again by an increase to 7.87 kU/l (P < 0.002) after 9 days of exposure. The evaluation of the kinetics of changes in nasal specific IgE revealed a significant decrease (P < 0.01) as soon as antigen avoidance was implemented for 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

It is generally accepted that Lp(a) is an independent risk factor of cardiovascular diseases. Since the apolipoprotein component of Lp(a) shows some homologies to plasminogen, it is, however, unclear as to whether the pathological effect is due to the role played by the lipoprotein in lipid metabolism or in the fibrinolytic system. We compared two groups of patients with myocardial infarction, with and without angiographically documented coronary artery disease. In the latter group, imbalances in the clotting system are very likely, while members of the former group may also display disturbances of lipid metabolism. The results show that the two groups display differences in lipid metabolism, whereas they have similar patterns of thrombogenicity indices and Lp(a) values. This study seems to support the hypothesis that Lp(a) does play a role in the fibrinolytic system, since even those myocardial infarctions without obstructive coronary artery disease have a high frequency of Lp(a) concentrations above 300 mg/l, i.e. similar to the situation found in the myocardial infarctions with angiographically documented coronary artery disease. Whether the high Lp(a) concentrations in the two groups are related to an impaired fibrinolysis will be the subject of further investigation.

Myocardial ischemia with normal coronary arteries can be due to anatomic or functional reasons. The more severe congenital coronary anomalies in the adulthood are the origin of the left main of the left coronary artery from the right aortic sinus, with a course between the aorta and the pulmonary trunk, and the origin of the left main from the pulmonary trunk. Both these anomalies can cause sudden death, usually associated with physical exertion. The coronary vasomotion of epicardial vessels depends on the interaction of several neurohumoral substances. We report the hemodynamic, angiographic and stress test data of 30 patients affected by chest pain, with myocardial ischemia and normal coronary arteries. In 8 patients the response of epicardial coronary arteries to intracoronary infusion of acetylcholine was evaluated.

Myocardial infarction and normal coronary arteries is not a rare event in the ischemic heart disease. Even if the patients with acute myocardial infarction and angiographically normal coronary arteries represent a small percentage (reported incidence varies from 1% to 12%) of all patients with acute ischemic attacks, they might be useful to highlight the pathogenetic mechanisms of this syndrome. To improve the understanding of this clinical entity, we reviewed our experience of 18 patients with myocardial infarction and normal coronary arteries. They were compared with a control group of patients with similar clinical characteristics (gender, age, infarct location) and residual coronary artery stenosis. The myocardial damage was less extensive in patients without residual stenosis (peak CK-MB: 56.1 +/- 71.9 vs 126.5 +/- 87.9 IU/I, p < 0.05), with a better left ventricular function either global (ejection fraction: 64 +/- 11 vs 55 +/- 13%, p < 0.05) and regional (SD/chord: -1.36 +/- 1.20 vs -2.42 +/- 1.04, p < 0.02). These findings probably reflect a more prompt and complete reperfusion of the infarct related artery. Myocardial necrosis may occur without obstructive coronary artery disease by the interaction of multiple factors such as abnormal platelet aggregation, thrombus formation and localized or diffuse changes of coronary vascular tone.

The contrast agent SHU-454 was intravenously injected in 103 patients during echocardiography: 37 mL/patient +/- 7 ml/patient. The quality of the contrast effect was optimal in 13, good in 51, sufficient in 30, and poor in 9 patients; reproducibility was optimal in 38, good in 46, sufficient in 17, and poor in 2 patients. Taste sensation, arm discomfort, or atypical chest pain occurred in 5 patients, premature ventricular contractions in 3. An isolated anginal attack occurred in 1 patient with frequent episodes at rest. A slight reduction in hematologic indices was attributed to hemodilution. Thus, SHU-454 produces a good and reproducible contrast effect with tolerable side effects.

Thirteen biochemical markers of infection and inflammation were measured during anti-Pseudomonas therapy in cystic fibrosis (CF) patients with respiratory exacerbation. The assessment of some of these markers is thought to be helpful in the evaluation of efficacy of antibiotic therapy in CF.

Seventeen of the centres participating to the G.I.S.S.I. trial performed also, before discharge from the Hospital, an echocardiographic examination of patients (pts) included in the study. 561 pts were included, 280 assigned to the streptokinase (SK) treatment, and 281 to the control (CT) group. The echocardiographic asynergic area score index was lower in the SK pts than in the CT group (p less than 0.01). The difference was more evident in pts treated within 6 hours from the onset of symptoms (p less than 0.005), in pts without previous infarct (p less than 0.005), and in pts aged over 65 (p less than 0.005). The end diastolic (EDV) and the end-systolic (ESV) volumes were lower in SK pts (p less than 0.01 and p less than 0.025 respectively) than in the CT group; the ejection fraction (EF) did not differ. The reduction of EDV and ESV was more evident in pts treated within 6 hours, in pts without previous infarct, in pts aged over 65, and in anterior infarcts. At the 6-month follow-up examination, in SK pts the asynergic area score index, the EDV, the ESV and the EF were unmodified; in CT pts, on the contrary, the EDV and the ESV were significantly increased (p less than 0.05 and p less than 0.025 respectively).

It has been shown that streptokinase administration at the time of acute myocardial infarction reduces mortality significantly, and that this reduction in mortality should be related to salvage of jeopardized myocardium and preservation of left ventricular function. To better define the relation between thrombolytic therapy and left ventricular modeling and function after acute myocardial infarction, 331 consecutive patients enrolled in the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico trial were studied by two-dimensional echocardiography just before discharge from the hospital. A 6 month follow-up examination was also available in 232 of these patients. Ventricular volumes were computed from an apical four chamber view, according to a previously published algorithm. An infarct size index was also semiquantitatively assessed, according to the number of akinetic and dyskinetic segments in an 11 segment left ventricular model. At predischarge examination, the 161 patients assigned to streptokinase treatment showed smaller ventricular volumes (end-diastolic volume 119.3 +/- 49.7 versus 134.5 +/- 57.8 ml [p = 0.011]; end-systolic volume 65.4 +/- 36.4 versus 74.9 +/- 45.7 ml [p = 0.036]) and smaller regional wall motion index (2.2 +/- 1.9 versus 2.7 +/- 1.9 segments; p = 0.019) compared with values in the 170 patients assigned to standard care; there was no difference in ejection fraction (46.6 +/- 14.1 versus 45.9 +/- 14.9%; p = 0.64). For both groups of patients, there was a significant relation between end-systolic volume and regional wall motion index (p less than 0.001); for large and similar extents of infarct size, ventricular volume was smaller in patients assigned to thrombolytic treatment than in patients assigned to standard care. At 6 months' follow-up, the differences in volume and regional dysfunction detected at the early examination persisted: 110.8 +/- 47.6 versus 127.9 +/- 53.8 ml for end-diastolic volume (p = 0.001), 56.3 +/- 33.6 versus 69.4 +/- 42.1 ml for end-systolic volume (p = 0.001) and 1.8 +/- 1.8 versus 2.3 +/- 1.8 segments for regional wall motion index (p = 0.001). Again, for comparable extents of infarct size, end-systolic volume was smaller in patients who received streptokinase (n = 110) than in those assigned to conventional treatment (n = 122). It is concluded that streptokinase improves left ventricular modeling and function in patients with myocardial infarction, reducing the extent of regional wall motion abnormalities and lessening postinfarction ventricular dilation. The beneficial effects persist up to 6 months.

The echocardiographic features of a case of postinfarction pseudoaneurysm of the left ventricle are described. M-mode echocardiography displayed an echo-free space behind the posterior left ventricular wall and two-dimensional echocardiography defined the saccular contour of the pseudoaneurysm and its probable communication with the ventricular cavity. A second echocardiographic examination--a week later--revealed a marked enlargement of the pseudoaneurysm and a characteristic fast backward early systolic motion of the ventricular wall interposed between left ventricular cavity and the saccular aneurysm; this motion is interpreted as a passive displacement of the ruptured wall during ventricular systole, and allows a differential diagnosis with similar echocardiographic M-mode aspects, due to pericardial effusion, pleural effusion or pericardial cysts. Echocardiography findings were confirmed by angiocardiography and the surgery. Echocardiography seems to be a safe method for early non-invasive diagnosis of left ventricular pseudoaneurysm.

Doppler left ventricular inflow time-velocity curves have been extensively used to evaluate left ventricular filling. The reproducibility of the technique, however, has been rarely assessed, its temporal variability being, presently, unknown. In order to define the temporal reproducibility of Doppler parameters of left ventricular filling, 10 normal subjects were studied at 3 different times (baseline, after 24 hours, and after 1 week). No parameter changed significantly during 1 week follow-up. When variability, however, was expressed as percent changes relative to baseline, values ranging from 5.7% to 25% were found, the largest variability being associated with acceleration-deceleration parameters (p less than 0.001). In conclusion temporal variability of parameters obtained from Doppler diastolic mitral time-velocity curves is acceptable in homogeneous groups of subjects. When the technique, however, is used for serial evaluation of ventricular filling in a single patient, the specific temporal variability of the parameter considered must be taken into account before any variation can be ascribed to real hemodynamic changes.

The long-term antianginal effect of orally administered verapamil over 1 year of continuous treatment was assessed in 11 patients with effort-induced angina. In the short-term phase of the study, patients were given, in random order, placebo and verapamil (360 mg/day). The tolerated work load during a bicycle exercise test was 531.8 +/- 123.0 kg/min on placebo and 763.6 +/- 124.7 kg/min on verapamil (p less than 0.001). Subsequently all patients entered a long-term study of 1-year continuous treatment with 120 mg t.i.d. verapamil. The tolerated work load at 8-week (736.4 +/- 105.1 kg/min) and 1-year (804.6 +/- 101.1 kg/min) tests did not significantly differ from the results in the short-term study. The average verapamil plasma level was 138.5 +/- 90.6 ng/ml before and 357.8 +/- 199.2 ng/ml 90 min after drug administration; the average norverapamil plasma levels were, respectively, 248.0 +/- 84.4 and 368.0 +/- 135.9 ng/ml. There was no correlation between verapamil or norverapamil plasma concentrations and the antianginal effect. No patient developed signs of heart failure during the treatment. Two patients had mild constipation. The average P-R interval was slightly, although significantly (p less than 0.01) prolonged, but no patient developed first-degree atrioventricular block. We conclude that verapamil proves an effective and safe drug in the treatment of effort-induced angina; the beneficial effects of the short-term treatment are sustained during 1 year of continuous treatment.

The anti-anginal effect of oral verapamil was assessed in 12 patients with chronic effort-induced angina, using a single-blind, placebo-controlled protocol. The patients were given, in random order, placebo, verapamil 240 mg/day, verapamil 360 mg/day, for 24 hours, followed by a 24-hour washout period. Increase in tolerated work load, compared to a baseline bicycle exercise test, was -25 +/- 55.9 kgm/min on placebo, 137.5 +/- 96 on verapamil 240 mg/day, 212.5 +/- 129.3 on verapamil 360 mg/day (p less than 0.001). While taking verapamil in 9 patients 240 mg/day the test was interrupted with of ECG alterations; at the same work load, only 1 patient had ECG alterations while taking verapamil 360 mg/day (p less than 0.01) and 9 completed the test without ECG alterations. The pressure-rate product at maximum exercise was not significantly affected by treatments. The higher dosage of verapamil prolonged the P-R interval (p less than 0.01) but only 1 patient had first-degree AV block. It is concluded that verapamil is a powerful and safe drug in the treatment of effort-induced angina: there is evidence that the effect depends on the dosage administered.